Changes in lipid profile over 24 months among adults on first-line highly active antiretroviral therapy in the home-based AIDS care program in rural Uganda.

BACKGROUND: Use of highly active antiretroviral therapy (HAART) has been linked to dyslipidemia and increased risk of cardiovascular disease (CVD) in HIV-infected patients in industrialized countries. The effects of HAART on lipid metabolism among sub-Saharan Africans, for whom access to antiretroviral therapy is expanding, remain largely unknown.
METHODS: From July 2003 to May 2004, 987 antiretroviral-naive patients with symptomatic HIV disease or a CD4 count <250 cells/mm3 were started on HAART in the Home-Based AIDS Care (HBAC) Program in Tororo, Uganda. The HBAC Program provided weekly drug delivery and field-based clinical monitoring. Nonfasting repository sera from a subset of 374 patients were analyzed for levels of total cholesterol (TC), direct low-density lipoprotein cholesterol (LDL-c), direct high-density lipoprotein cholesterol (HDL-c), and triglycerides (TG) at baseline (before HAART) and after 12 and 24 months of HAART using Randox enzymatic kits (Crumlin, United Kingdom).
RESULTS: The 374 patients evaluated (49% women, mean age = 39 years, CD4 count = 124 cells/mm3, body mass index = 19.7 kg/m2) received initial HAART composed of stavudine, lamivudine, and either nevirapine (365 patients [98%]) or efavirenz (9 patients [2%]). During 24 months, 99 (26%) patients had single drug substitutions from stavudine to zidovudine and 27 (7%) had single drug substitutions from nevirapine to efavirenz. At baseline, the mean serum lipid concentrations were 120 mg/dL for TC, 53 mg/dL for LDL-c, 29 mg/dL for HDL-c, and 123 mg/dL for TG; values were generally comparable for men and women. During 24 months of treatment, TC increased by a mean of 31 mg/dL, LDL-c by a mean of 26 mg/dL, and HDL-c by a mean of 19 mg/dL, whereas the TC/HDL-c ratio decreased from a mean of 4.6 to 3.4 (all changes, P < 0.001). TG levels initially decreased and then returned to baseline levels by 24 months. At baseline and 24 months, respectively, TC was > or =200 mg/dL for 2% and 10% of patients, LDL-c was > or =130 mg/dL for 1% and 6%, HDL-c was <40 mg/dL for 88% and 41%, and TG were > or =150 mg/dL for 23% and 20%.
CONCLUSIONS: Rural Ugandans with advanced HIV disease initiating nevirapine- or efavirenz-based HAART experienced infrequent elevations in TC, LDL-c, and TG at baseline and after 24 months of therapy. Increases in HDL-c levels were substantial and proportionally greater than increases in TC or LDL-c levels. The risk of CVD and how it is affected by lipid changes in this rural African population are unknown. However, the changes we observed after 24 months of HAART seem unlikely to increase the risk of CVD.